Rapid communicationInvolvement of calcineurin in glutamate-induced mitochondrial dynamics in neurons
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Acknowledgment
This work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan.
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Glutamate antagonism fails to reverse mitochondrial dysfunction in late phase of experimental neonatal asphyxia in rats
2011, Neurochemistry InternationalElevated intracellular calcium causes distinct mitochondrial remodelling and calcineurin-dependent fission in astrocytes
2011, Cell CalciumCitation Excerpt :While this measurement could potentially be affected by mitochondria moving into, or out of the peripheral region selected for analysis, this is unlikely to have a significant impact upon the relative numbers of mitochondria, given that the motility of mitochondria was not significantly different at all time intervals analyzed (Fig. 4). A recent study reported that calcineurin inhibitors attenuated glutamate-mediated reductions in mitochondrial length and movement in hippocampal neurons [21]. In the present study we did not observe a significant effect of calcineurin inhibitors on Ca2+-mediated changes in mean mitochondrial length, only a direct effect on net fission events.
H<inf>2</inf>O<inf>2</inf>-induced mitochondrial fragmentation in C<inf>2</inf>C<inf>12</inf> myocytes
2010, Free Radical Biology and MedicineCitation Excerpt :By visualizing cells with CLSM after 250 μM H2O2 pretreatments of various durations (from 5 min to 6 h), we found that fragmentation proceeded slowly, peaking at 5.5 h with 250 μM H2O2 (Fig. 2C). In consideration of previous findings of rapid fragmentation caused by various stimuli in other cell types [7,9,31–33], we sought to determine whether there could be “fast” fragmentation in C2C12 myocytes. We found that although the respiratory uncoupler CCCP had no effect at 100 nM even after 15 min, 10 μM CCCP induced cytosolic MitoTracker leakage and the appearance of numerous punctiform mitochondria within 3 min of its addition to live cells (Fig. S6).
Regulation of mitochondrial fission by intracellular Ca<sup>2+</sup> in rat ventricular myocytes
2010, Biochimica et Biophysica Acta - BioenergeticsCitation Excerpt :It may be possible that hFis1, which has been shown to regulate DLP1 recruitment and assembly, may interact with inner mitochondrial proteins or membrane spanning protein complexes that are regulated by Ca2+. However, Ca2+ signaling pathways in the cytosol have been shown to regulate mitochondrial morphology via phosphorylation and dephosphorylation of DLP1 [47–52]. Future experiments will be necessary to elucidate how mitochondrial Ca2 increase activates the mitochondrial fission machinery, and if this is a different pathway than DLP1 activation.
Complexity of mitochondrial dynamics in neurons and its control by ADP produced during synaptic activity
2009, International Journal of Biochemistry and Cell BiologyCaspase-cleaved tau expression induces mitochondrial dysfunction in immortalized cortical neurons: Implications for the pathogenesis of alzheimer disease
2009, Journal of Biological ChemistryCitation Excerpt :For example, FK506-induced inhibition of calcineurin efficiently prevents the loss of mitochondrial membrane potential in glutamate-treated astrocyte cultures (48). In addition, treatment of hippocampal neurons with glutamate resulted in inhibition of mitochondrial movement and a decrease in mitochondrial length, which were prevented by inhibiting calcineurin either with FK506 or CsA (49). Although the data indicate that T4C3 induces mitochondrial fragmentation through activation of calcineurin, further studies are required to elucidate the mechanisms.